Possible value of galectin-3 on follow-up of cardiac remodeling during glucocorticoid treatment

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dc.authoridAkin, Senay/0000-0001-5729-5944
dc.authoridGURAY, UMIT/0000-0002-6604-2970
dc.authoridDemirel, Haydar/0000-0003-3334-4793
dc.contributor.authorAkin, Senay
dc.contributor.authorKubat, Gokhan B.
dc.contributor.authorGuray, Umit
dc.contributor.authorAkin, Yesim
dc.contributor.authorDemirel, Haydar A.
dc.date.accessioned2024-09-29T15:50:42Z
dc.date.available2024-09-29T15:50:42Z
dc.date.issued2021
dc.departmentKarabük Üniversitesien_US
dc.description.abstractGlucocorticoids are among the most prescribed drugs globally due to their potent anti-inflammatory and immunosuppressive properties. Although they have positive effects on the treatment of various disease states; long-term administration is associated with high blood pressure, insulin resistance, and susceptibility to type 2 diabetes. The heart attempts to cope with increased blood pressure and a decrease in glucose utilization by developing pathological cardiac remodeling. However, in this process, cardiac fibrosis formation and deterioration in heart structure and functions occur. Galectin-3, a member of the beta-galactoside binding lectins, is consistently associated with inflammation and fibrosis in the pathogenesis of various disease states including insulin resistance and heart failure. Galectin-3 expression is markedly increased in activated macrophages and a subset of activated fibroblasts and vascular cells. Also, failing and remodeling myocardium show increased Gal-3 expression and elevated Gal-3 levels are related to heart failure severity and prognosis. Furthermore, Gal-3-related pathways are recently suggested as therapeutic targets both pharmacologically and genetically to increase insulin sensitivity in vivo. The objective of this review is to provide a summary of our current understanding of the role of glucocorticoid-associated insulin resistance, which is important for some cardiac events, and the potential role of galectin in this pathophysiological process.en_US
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK) [219S175]en_US
dc.description.sponsorshipThis study was supported by the Scientific and Technological Research Council of Turkey (TUBITAK) (Grant No: 219S175).en_US
dc.identifier.doi10.1002/jbt.22717
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue4en_US
dc.identifier.pmid33484019en_US
dc.identifier.scopus2-s2.0-85099763396en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1002/jbt.22717
dc.identifier.urihttps://hdl.handle.net/20.500.14619/3697
dc.identifier.volume35en_US
dc.identifier.wosWOS:000610912500001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Biochemical and Molecular Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectcardiac functionsen_US
dc.subjectdexamethasoneen_US
dc.subjectfibrosisen_US
dc.subjectinsulin signalingen_US
dc.titlePossible value of galectin-3 on follow-up of cardiac remodeling during glucocorticoid treatmenten_US
dc.typeArticleen_US

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